2026-04-14T21:06:05Zhttps://uvadoc.uva.es/oai/requestoai:uvadoc.uva.es:10324/656072025-03-26T19:10:04Zcom_10324_1145com_10324_931com_10324_894col_10324_1254
UVaDOC
author
Bolaños, Juan P.
author
García Nogales, Paula
author
Vega Agapito, María Victoria
author
Delgado Esteban, María
author
Cidad Velasco, María Del Pilar
author
Almeida, Angeles
2024-02-02T22:55:37Z
2024-02-02T22:55:37Z
2001
Progress in Brain Research
https://uvadoc.uva.es/handle/10324/65607
10.1016/S0079-6123(01)32094-0
441
454
132
Nitric oxide (žNO) is a highly diffusible, short-lived
physiological messenger present in the central nervous
system (CNS) (Garthwaite et al., 1988) that
is synthesised by a family of nitric oxide synthases
(NOSs) which catalyze the conversion of arginine
to citrulline and žNO (Bredt and Snyder, 1990;
Knowles and Moncada, 1994). All CNS cells synthesise
žNO (Murphy et al., 1993). Neurones produce
žNO by calcium-dependent activation of neuronal,
constitutive NOS (nNOS or NOS1), whereas glial
cells synthesise žNO in a calcium-independent way
that requires previous transcriptional induction of
NOS (inducible NOS, iNOS or NOS2) (Galea et al.,
1992; Simmons and Murphy, 1992). Astrocytes also
synthesise žNO through NNOS activity (Murphy et
al., 1990, 1991; Agullo´ andGarcı´a, 1992a,b). A third
isoform of NOS (endothelial NOS, eNOS or NOS3)
is associated with brain vasculature.
In general, žNO participates in the transduction
pathway leading to elevations in intracellular cyclic
Ł Corresponding author: Dr. Juan P. Bolan˜os, Departamento
de Bioquı´mica y Biologı´a Molecular, Universidad
de Salamanca, Edificio Departamental, Plaza Doctores
de la Reina s=n, 37007 Salamanca, Spain. Tel.:
C34-923-294526; Fax: C34-923-294579;
E-mail: jbolanos@gugu.usal.es
GMP levels (Bredt and Snyder, 1989; Knowles et
al., 1989) and therefore participates in cyclic GMP
functions (Wang and Robinson, 1997). However, an
increasing body of evidence is now arising to suggest
that žNO and its most active metabolite, the peroxynitrite
anion (ONOO ), may be involved in the regulation
of brain energy metabolism. This chapter will
specifically focus on the mechanisms involving žNO
and ONOO -mediated interference with brain mitochondrial
energy production and the modulating role
of glutathione in cell energy metabolism. Finally, we
discuss recent evidence that strongly suggests the
importance of cell glucose utilisation in maintaining
glutathione homeostasis and hence in preventing
nitric oxide-mediated mitochondrial impairment.
eng
Nitric oxide-mediated mitochondrial impairment in neural cells: a role for glucose metabolism in neuroprotection
info:eu-repo/semantics/article
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